HORMONE CONTROL

OF GROWTH
Dedi ardinata
Yetty Machrina
PHYSIOLOGY DEPARTMENT OF
MEDICAL SCHOOL
UNIVERSITAS SUMATERA UTARA

GROWTH

organized addition of new tissue that occurs

normally in development from infancy to
adulthood

This process is complex and depends on

the interplay of genetic, nutritional, and
environmental influences as well as actions
of the endocrine system (paracrine or
autocrine mechanisms)

Patterns of growth and development during

childhood and adolescence

The rapid rate of growth seen in fetal life

continues into the postnatal period but
declines significantly through early
childhood. There is further deceleration
prior to the growth spurt of puberty.

GROWTH HORMONE

Growth hormone (GH), which is also called

somatotropin (STH), is the single most
important hormone for normal growth.
Attainment of adult size is absolutely
dependent on GH, in its absence, growth is
severely limited, and when it is present in
excess, growth is excessive.
GH as the facilitator of expression of
genetic potential for growth

GH produced by somatotropes from anterior

pituitary
Structural similarity to prolactin and Human
Placental Lactogen binds to its receptor on the
surface of target cells.
Growth Hormone Releasing Hormone from
hypothalamus control secretion of GH while
somastatin inhibit it.
GH secretion shows irregular pulsatile release,
influenced by physiological stimuli, such as
stress and exercise
Growth hormone is secreted about every 3
hours

There is a significant increase rate of

secretion during slow wave (deep) sleep,
and nocturnal sleep particularly in children.

EFFECT ON SKLETAL GROWTH

The ultimate height attained by an

individual is determined by the length of the
skeleton, in particular the vertebral column
and long bones of the legs
Growth of these bones occurs by a process
called endochondral ossification, in which
proliferating cartilage is replaced by bone

GH act in epiphyseal plates influence

celluler proliferation causes columns of
chondrocytes to elongate and epiphyseal
plates to widen
In the absence of GH there is severe
atrophy of the epiphyseal plates, which
become narrow as proliferation of cartilage
progenitor cells slows markedly

After epiphyses fused, growth has

stopped
Low rates of GH secretion in the elderly
may be related to loss of lean body mass
in later life.
Growth hormone stimulates growth of the
long bones by stimulating production of
insulin-like growth factor I (IGF-I).

Insulin-like growth factor I produced locally

and in the liver stimulates growth and
maturation of chondrocytes in epiphysial
plates.
Growth hormone increases lean body
mass, decreases body fat, promotes fatty
acid utilization, and limits carbohydrate
utilization.

THYROID HORMONE

Thyroid hormone is required by the

somatotrope for normal GH synthesis and
secretion.
Thyroid hormones maintain tissue sensitivity to
GH and IGF-I and hence are required for
normal expression of GH actions.
Hyperthyroidism in childhood increases the
rate of growth, but, because of early closure of
the epiphyses, the maximum height attained is
not increased

Failure of growth in thyroid-deficient individuals is

largely due to a deficiency of GH, which may be
compounded by a decrease in sensitivity to GH
Thyroid hormones
Increase expression of GH receptors in rodent
tissues. T3 and T4 also potentiate effects of GH
on the growth of long bones and increase its
effects on protein synthesis in muscle and liver.

INSULIN

Optimal concentrations of insulin in blood are required

to maintain normal growth during postnatal life
Growth is often retarded in insulin-dependent diabetic
children
Studies in pancreatectomized rats indicate a direct
relation between the effectiveness of GH and the dose
of insulin administered.
GH sustained a rapid rate of growth as long as the daily
dose of insulin was adequate, but growth progressively
decreased as the dose of insulin was reduced

SEX HORMONE

Androgen secretion during puberty in boys

produces a doubling of muscle mass by
increasing the size and number of muscle
cells.
Both androgen and estrogens increase GH
secretion
The pubertal growth spurt results from
increased amplitude of GH secretory pulses
induced by gonadal steroid hormones.

Estrogens hasten epiphyseal closure and

therefore limit growth.
Androgens directly stimulate growth of soft
tissue (e.g., muscle).
At the same time that gonadal steroids
promote linear growth, they accelerate
closure of the epiphyses and therefore limit
the final height that can be attained

GLUCOCORTICOID

Glucocorticoids are required for synthesis of GH

and have complex effects on GH secretion
They may enhance GH gene transcription and
increase responsiveness of somatotropes to
GHRH.
GH secretion is reduced by excessive
glucocorticoids, probably as a result of increased
somatostatin production.
Glucocorticoids also antagonize the actions of GH
for their catabolic effect

HORMONE CONTROL OF GROWTH

DISORDERS

Pituitary dwarfism is the failure of growth that results

from lack of GH during childhood
Overproduction of GH during childhood results in
gigantism
Overproduction of GH during adulthood, after the
growth plates of long bones have fused There is
thickening of the cranium and mandible, as well as
enlargement of some facial bones and bones in the
hands and feet, names acromegaly
Children suffering from overproduction of
glucocorticoids(Cushings disease) experience
some stunting of their growth